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Mental disorders account for at least 18% of global disease burden, and the associated annual global costs are projected to be US$6 trillion by 2030. Evidence-based, cost-effective public mental health (PMH) interventions exist to prevent mental disorders from arising, prevent associated impacts of mental disorders (including through treatment), and promote mental wellbeing and resilience. However, only a small proportion of people with mental disorders receive minimally adequate treatment. Compared with treatment, there is even less coverage of interventions to prevent the associated impacts of mental disorders, prevent mental disorders from arising, or promote mental wellbeing and resilience. This implementation failure breaches the right to health, has increased during the COVID-19 pandemic, and results in preventable suffering, broad impacts, and associated economic costs. In this Health Policy paper, we outline specific actions to improve the coverage of PMH interventions, including PMH needs assessments, collaborative advocacy and leadership, PMH practice to inform policy and implementation, training and improvement of population literacy, settings-based and integrated approaches, use of digital technology, maximising existing resources, focus on high-return interventions, human rights approaches, legislation, and implementation research. Increased interest in PMH in populations and governments since the onset of the COVID-19 pandemic supports these actions. Improved implementation of PMH interventions can result in broad health, social, and economic impacts, even in the short-term, which support the achievement of a range of policy objectives, sustainable economic development, and recovery.

Following approval of the ICD‐11 by the World Health Assembly in May 2019, World Health Organization (WHO) member states will transition from the ICD‐10 to the ICD‐11, with reporting of health statistics based on the new system to begin on January 1, 2022. The WHO Department of Mental Health and Substance Abuse will publish Clinical Descriptions and Diagnostic Guidelines (CDDG) for ICD‐11 Mental, Behavioural and Neurodevelopmental Disorders following ICD‐11’s approval. The development of the ICD‐11 CDDG over the past decade, based on the principles of clinical utility and global applicability, has been the most broadly international, multilingual, multidisciplinary and participative revision process ever implemented for a classification of mental disorders. Innovations in the ICD‐11 include the provision of consistent and systematically characterized information, the adoption of a lifespan approach, and culture‐related guidance for each disorder. Dimensional approaches have been incorporated into the classification, particularly for personality disorders and primary psychotic disorders, in ways that are consistent with current evidence, are more compatible with recovery‐based approaches, eliminate artificial comorbidity, and more effectively capture changes over time. Here we describe major changes to the structure of the ICD‐11 classification of mental disorders as compared to the ICD‐10, and the development of two new ICD‐11 chapters relevant to mental health practice. We illustrate a set of new categories that have been added to the ICD‐11 and present the rationale for their inclusion. Finally, we provide a description of the important changes that have been made in each ICD‐11 disorder grouping. This information is intended to be useful for both clinicians and researchers in orienting themselves to the ICD‐11 and in preparing for implementation in their own professional contexts.

Supplemental digital content is available in the text.In this study, we sought to examine factors associated with dosing of antidepressants (ADs) in Asia. Based on reported data and clinical experience, we hypothesized that doses of ADs would be associated with demographic and clinical factors and would increase over time. This cross-sectional, pharmacoepidemiological study analyzed data collected within the Research Study on Asian Psychotropic Prescription Pattern for Antidepressantsfrom 4164 participants in 10 Asian countries, using univariate and multivariate methods. The AD doses varied by twofold among countries (highest in PR China and RO Korea, lowest in Singapore and Indonesia), and averaged 124 (120–129) mg/d imipramine-equivalents. Average daily doses increased by 12% between 2004 and 2013. Doses were significantly higher among hospitalized patients and ranked by diagnosis: major depression > anxiety disorders > bipolar disorder, but were not associated with private/public or psychiatric/general-medical settings, nor with age, sex, or cotreatment with a mood stabilizer. In multivariate modeling, AD-dose remained significantly associated with major depressive disorder and being hospitalized. Doses of ADs have increased somewhat in Asia and were higher when used for major depression or anxiety disorders than for bipolar depression and for hospitalized psychiatric patients.

The aim of this study was to survey the use of antipsychotic polypharmacy (APP) in older Asian patients with schizophrenia and examine its demographic and clinical correlates.

There is little information available concerning the possible effects of ascorbic acid on glucose-6-phosphate dehydrogenase (G-6-PD) - deficient erythrocytes. We therefore studied the survival of G-6-PD- deficient cells, incubated with ascorbic acid, in rats with partial reticuloendothelial and complement blockade. Animals were pretreated with ethyl palmitate and cobra venom factor. They were then transfused with 51Cr-labeled erythrocytes which had been incubated in the presence or absence of ascorbic acid. G-6-PD-deficient cells, incubated with ascorbic acid, had impaired survival when compared to that of controls. G-6-PD-deficient cells, in the absence of ascorbic acid, had survival times equal to those of normal control erythrocytes. At the concentrations used, ascorbic acid did not appear to alter the survival of normal cells. Ascorbic acid causes premature loss of G-6-PD- deficient human erythrocytes in this rat model. On the basis of previous clinical and experimental observations, as well as this study, caution should be used when administering ascorbic acid in large doses to individuals who might be G-6-PD deficient.

First-night effects (FNE) were comparatively investigated in patients with disorders in initiating and maintaining sleep (DIMS) associated with generalized anxiety disorder (GAD) in laboratory (n = 22) and home sleep polysomnography (n = 21). Patients had to be drug-free for at least 2 weeks prior to the first recording. Evaluation measures included 1) objective data on sleep initiation and maintenance; 2) sleep architecture based on polysomnographic recordings, analyzed visually according to the criteria of Rechtschaffen and Kales; 3) subjectively estimated sleep and awakening quality, assessed by a self-rating scale and visual analogue scales; 4) objective awakening quality as measured by a psychometric test battery; and 5) psychophysiological data, including critical flicker frequency, muscle strength, pulse, and blood pressure. Statistical analysis using multivariate analysis of variance (MANOVA) demonstrated multiple FNE in both groups regarding sleep efficiency, total sleep time, percentage of time in stage 2 sleep, percentage of time in stage 3/4 sleep, minutes of rapid eye movement (REM) sleep, and REM sleep latency. There was a group-by-night effect in the number of awakenings. There were no significant FNE regarding subjective sleep and awakening quality in either group. Differential adaptation effects were observed in attention and fine motor activity, with improvement in laboratory-recorded patients and deterioration in home-recorded patients. Differential findings also occurred in regard to evening blood pressure, with laboratory-recorded patients showing more adaptation.

There is little information available concerning the possible effects of ascorbic acid on glucose-6-phosphate dehydrogenase (G-6-PD) -deficient erythrocytes. We therefore studied the survival of G-6-PD-deficient cells, incubated with ascorbic acid, in rats with partial reticuloendothelial and complement blockade. Animals were pretreated with ethyl palmitate and cobra venom factor. They were then transfused with 51Cr-labeled erythrocytes which had been incubated in the presence or absence of ascorbic acid. G-6-PD-deficient cells, incubated with ascorbic acid, had impaired survival when compared to that of controls. G-6-PD-defìcient cells, in the absence of ascorbic acid, had survival times equal to those of normal control erythrocytes. At the concentrations used, ascorbic acid did not appear to alter the survival of normal cells. Ascorbic acid causes premature loss of G-6-PD-defìcient human erythrocytes in this rat model. On the basis of previous clinical and experimental observations, as well as this study, caution should be used when administering ascorbic acid in large doses to individuals who might be G-6-PD deficient.

Introduction: In 2000, the Thai Ministry of Public Health appointed a taskforce to revise the International Statistical Classification of Diseases and Relate Health Problems 10th Revision (ICD‐10) to make it more suitable for use in Thailand: the ICD‐10 Thai Modification (ICD‐10 TM).